Burkitt lymphoma—one of the most aggressive tumors—may be treatable with agents that can stop cell proliferation and induce cell death by reactivating two key proteins.

Such a possibility has been spawned by a recent discovery regarding a genetic locus that has an important role in Burkitt lymphoma. The INK4a/ARF locus encodes two important tumor-suppressor proteins: p16 (INK4a) and p14 (ARF). Genetic mutations usually serve to inactivate these two proteins in human tumors, allowing cells to proliferate uncontrollably.

Now, a research team based at the Sbarro Health Research Organization Center for Biotechnology at Temple University in Philadelphia has discovered that in Burkitt lymphoma, the locus is genetically unchanged, but epigenetic and posttranscriptional mechanisms inactivate the product proteins.

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“Since in Burkitt lymphoma these two proteins [INK4a and ARF] are not inactivated at the genetic level, their inactivation could be pharmacologically reversible,” explained lead author Annalisa Roberti in a statement describing her group’s findings, which were reported in the journal Cell Cycle (2011;10[1]:127-134). “The reactivation of p16 and p14 in our model and our ability to inhibit cell proliferation and induce apoptosis through the Rb- and p-53 pathways opens new prospects for the understanding and treatment of Burkitt lymphoma.”